We will use a K sensitive electrode to record extracellular (AoK) and intracellular (AiK) K activity in canine Purkinje fiber and ventricular muscle, and to study the electrophysiology of Na-K ATPase in preparations of normal and abnormal tissue. We will record AoK curves during and after rapid beating (undershoot in AoK after rapid beating reflects Na-K ATPase activity) and then perform the following; 1) To evaluate the Na pump lag, we will quantitatively analyze the time constant and magnitude of AoK accumulation, decay and undershoot with rapid beating using Na-K ATPase blockers and various programs of stimulus trains (e.g. 2 stimulus trains in close succession). 2) To examine electrogenic Na extrusion we will perform prolonged rapid beating and record AoK, AiK, and Erest in varying K solutions. We will compare EK and Erest especially while varying extracellular K to the same EK level, at times of low (quiescent) and high (rapid beating) Na-K ATPase activity. We will evaluate the role of background Na leak current using Na leak current blockers and Na free solutions. 3) We will determine the effects of Na-K ATPase blockade (during rapid beating) on action potential parameters which are important in the genesis of arrhythmias (ERP, Vmax and APD of premature beats). 4) We will study 24 hour infarcted canine Purkinje fibers (in which diminished Na-K ATPase activity or increased background leak current could explain previously demonstrated electrophysiological alterations). We will determine whether Na-K diffusion, which may be altered in infarcted tissue, using K iontophoresis with a K recording electrode. 5) We will determine if there is activation of Na-K ATPase on rapid beating in slow response preparations with inward movement of Ca and not Na (the usual stimulus to Na-K ATPase). We will also correlate variations in AoK (which may be great if there is no Na-K ATPase stimulation) with conduction abnormalities in these preparations. The above studies will allow a better understanding of the nature of Na-K ATPase activity in cardiac tissue, its electrophysiological role and the role of Na-K ATPase changes in arrhymogenesis in models of depressed cardiac tissue resembling ischemia and infarction.